Value of cognitive fusion targeted and standard systematic transrectal prostate biopsy for prostate cancer diagnosis.

ABSTRACT: The aim of this study was to compare the accuracies of cognitive fusion-guided targeted biopsy (TB), systematic biopsy (SB), and combined TB+SB for the detection of prostate cancer (PCa) and clinically significant PCa (csPCa) in males with lesions detected by magnetic resonance imaging (MRI). We conducted a retrospective analysis of individuals who underwent prostate biopsy at Peking University People's Hospital (Beijing, China), with an emphasis on patients with both transrectal TB and SB. The main objective was to determine the precisions of SB, TB, and TB+SB for diagnosing PCa and csPCa. We also evaluated the detection rates of TB, SB, TB+ipsilateral-SB (ipsi-SB), TB+contralateral-SB (contra-SB), and TB+SB for PCa and csPCa in patients with unilateral MRI lesions. We compared the diagnostic yields of the various biopsy schemes using the McNemar's test. A total of 180 patients were enrolled. The rates of PCa detection using TB, SB, and TB+SB were 52.8%, 62.2%, and 66.7%, respectively, and the corresponding rates for csPCa were 46.1%, 56.7%, and 58.3%, respectively. Among patients with unilateral MRI lesions, the PCa detection rates for TB, SB, TB+ipsi-SB, TB+contra-SB, and TB+SB were 53.3%, 64.8%, 65.6%, 61.5%, and 68.0%, respectively. TB+ipsi-SB detected 96.4% of PCa and 95.9% of csPCa cases. These findings suggest that the combination of TB+SB has better diagnostic accuracy compared with SB or TB alone. For patients with unilateral MRI lesions, the combination of TB+ipsi-SB may be suitable in clinical settings.

Super-thin anterolateral thigh flap for reconstruction of the medial plantar artery perforator flap donor site.

BACKGROUND: The medial plantar artery perforator (MPAP) flap is widely used to reconstruct the weight-bearing area of the foot. Traditionally, its donor site is closed using a skin graft, which is associated with several complications, including walking disability. This study aimed to examine our experience with using a super-thin anterolateral thigh (ALT) flap to reconstruct the MPAP flap donor site. METHODS: We examined 10 patients who underwent reconstruction of the MPAP flap donor site using a super-thin ALT flap between August 2019 and March 2021. The vascular pedicle was anastomosed to the proximal end of the medial plantar vessels or the end of the posterior tibial vessels. RESULTS: All reconstruction flaps survived and all patients were satisfied with the aesthetic appearance. No blisters, ulcerations, hyperpigmentation, or contractures occurred. All patients gained protective sensation in the super-thin ALT flap. The average visual analog scale score for the aesthetic appearance of the reconstructed foot was 8.5 ± 0.7 (range, 8-10). All patients were able to ambulate without aids and could wear regular shoes. The average revised Foot Function Index score was 26.4 ± 4.1 (range, 22-34). CONCLUSION: Reconstruction of the MPAP flap donor site using a super-thin ALT flap is reliable and provides satisfactory functional recovery, aesthetic appearance, and protective sensation while minimizing postoperative morbidity.

Bruton tyrosine kinase (BTK) may be a potential therapeutic target for interstitial cystitis/bladder pain syndrome.

AIMS: To determine the potential diagnostic and therapeutic targets of Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS). METHODS: We selected the GSE11783, GSE57560 and GSE621 datasets from the GEO database and merged them. R software was used to screen differentially expressed genes (DEGs) between IC/BPS and normal bladder tissues. The "String" online tool is used to analyze DEGs interaction and functional protein enrichment. CIBERSORT online tool was used to analyze the infiltration of immune cells. In addition, we verified the function of BTK in IC/BPS at the clinical samples and cells level. RESULTS: Bioinformatics analysis revealed that 5 genes were significantly overexpressed in IC/BPS, and the protein-protein interaction diagram showed that BTK was a critical link between these five proteins. At the same time, functional enrichment showed that they were significantly related to innate immunity. Immunoinfiltration showed that mast cell resting in IC/BPS was significantly higher. IHC staining of clinical samples showed that the mast cell markers Tryptase and BTK were highly expressed in IC/BPS tissues. At the cell level, knockdown of BTK inhibited proliferation, migration, invasion, and degranulation of mast cells. CONCLUSIONS: This study provides a new perspective for understanding the molecular mechanisms involved in IC/BPS and suggests that BTK may be a target for treating IC/BPS.

Arthroscopic Treatment of Calcific Tendinitis of Gemellus Superior and Gemellus Inferior: A Case Report and Literature Review.

BACKGROUND: Tendon calcification is a common disease, and it could happen in the tendons of the shoulder, wrist, etc. However, tendon calcification in the superior and inferior gemellus is rare, and in this region is likely to be misdiagnosed. CASE PRESENTATION: Here, our case report first reported a 53-year-old female patient with an unusual case of calcific tendinitis of the gemellus superior and gemellus inferior muscles. The patient presented with severe pain in the right hip and lower extremities, not relieved using nonsteroidal anti-inflammatory drugs (NSAIDs). The preoperative physical examination indicated an abnormality in the hip joint. Preoperative imaging confirmed the results of the physical examination and showed a right hip lesion. We did not make a definite diagnosis preoperatively but considered that the patient might have an osteochondroma. However, surgical findings indicated that the lesion was not in the hip capsule on subsequent arthroscopic surgery, which suggested that the preoperative diagnosis might be wrong. We opened the posterior capsule and found a "toothpaste-like" lesion in the superior and inferior gemellus muscles' tendon. We thought this might be the calcified tendon. Then the arthroscopic surgery was finished to remove the lesion, and the removed tissue was sent to the pathology department for pathological examination. The pathological report confirmed the diagnosis of the calcified tendon. Postoperative follow-up was conducted. The effect of the operation was noticeable. Postoperative symptoms were relieved. CONCLUSIONS: Calcification of the tendons of the superior and inferior gemellus muscles can be easily misdiagnosed, and the disease can be treated minimally with arthroscopy.

[Advances in Pelvic Lymph Node Dissection for Bladder Cancer].

Bladder cancer has high morbidity and mortality rates worldwide. Its incidence is high in western countries and has shown an increasing trend in China. While radical cystectomy combined with pelvic lymph node dissection (PLND) is the standard treatment for bladder cancer,the optimal range of PLND remains controversial. In addition,the prognostic value of lymph node factors is also unclear. This article reviews research advances in PLND.

HYAL-1-induced autophagy facilitates pancreatic fistula for patients who underwent pancreaticoduodenectomy.

The main mechanism of hyaluronidase 1(HYAL-1) in the development of postoperative pancreatic fistula (POPF) after pancreatoduodenectomy (PD) was unknown. In this study, a comprehensive inventory of pre-, intra-, and postoperative clinical and biological data of two cohorts (62 pancreatic cancer [PCa] and 111 pancreatic ductal adenocarcinoma [PDAC]) which could induce POPF were retrospectively analyzed. Then, a total of 7644 genes correlated with HYAL-1 was predicted in PDAC tissues and the enriched pathway, kinase targets and biological process of those correlated genes were evaluated. Finally, a mouse pancreatic fistula (PF) model was first built and in vitro studies were performed to investigate the effects of HYAL-1 on PF progression. Our data indicated that preoperative serum HYAL-1 level, pancreatic fibrosis score, and pancreatic duct size were valuable factors for detecting POPF of Grade B and C. The serum HYAL-1 level of 2.07 mg/ml and pancreatic fibrosis score of 2.5 were proposed as the cutoff values for indicating POPF. The bioinformatic analysis and in vitro and in vivo studies demonstrated that HYAL-1 facilitates pancreatic acinar cell autophagy via the dephosphorylation of adenosine 5'-monophosphate-activated protein kinase (AMPK) and signal transducers and activators of transcription 3 (STAT3) signaling pathways, which exacerbate pancreatic secretion and inflammation. In summary, the preoperative serum HYAL-1 was a significant predictor for POPF in patients who underwent PD. Tumor-induced HYAL-1 is one of core risk in accelerating PF and then promoting pancreatic secretion and acute inflammation response through the AMPK and STAT3-induced autophagy.

[In vitro effect of all-trans retinoic acid on cell adhesion molecule expression and adhesion capacity of bone marrow stromal cells in patients received peripheral blood stem cell transplantation].

The aim of this study was to evaluate the effect of all-trans retinoic acid (ATRA) on cell adhesion molecule expression and adhesion capacity of bone marrow stromal cells (BMSC) in patients after conditioning treatment for peripheral blood stem cell transplantation (PBSCT). BMSC of 27 patients before and after conditioning treatment for PBSCT were cultured in vitro. After treated with ATRA at 0.01, 0.1, or 1 micromol/L, expression of intercellular adhesion molecule-1 (ICAM-1) protein and vascular adhesion molecule-1 (VCAM-1) protein were detected by flow cytometry, and soluble ICAM-1 (sICAM-1) protein was determined by using radioimmunoassay. Then BMSC was co-cultured with CD34+ cells, and adhesion rate of BMSC to CD34+ cells was measured. The results showed that after pretreatment with conditioning regimen for PBSCT, the expressions of ICAM-1 and VCAM-1 proteins in BMSC and the expression level of sICAM-1 protein in supernatant of BMSC culture were down-regulated, and the adhesion rate of BMSC to CD34+ cells was decreased, after administration of ATRA, the expression of ICAM-1 protein in BMSC, sICAM-1 protein in culture medium and adhesion rate of BMSC to CD34+ cells all increased significantly, but expression of VCAM-1 protein changed no significantly. It is concluded that the ATRA can partly restore adhesion function of BMSC injured by pretreatment for PBSCT and contribute to hematopoietic reconstitution.

Antagonist peptides of human interferon-alpha2b isolated from phage display library inhibit interferon induced antiviral activity.

AIM: To screen human interferon (IFN)-alpha2b antagonist peptides from a phage displayed heptapeptide library. METHODS: WISH cells and polyclonal anti-IFN-alpha2b antibodies were used to select IFN receptor-binding peptides from a phage displayed heptapeptide library. The specific binding of phage clones was examined by phage ELISA and immunohistochemistry. The specific binding activities of synthetic peptides to WISH cells were detected by competition assay. Effects of synthetic peptides to IFN-induced antiviral activity were analyzed by evaluating the cytopathic effect (CPE) using the MTT method. RESULTS: Twenty-three positive clones were obtained after seven rounds of selection. Ten clones were randomly picked from the positive clones and were sequenced. The corresponding amino acid sequences suggested 3 groups homologous to the 3 domains of IFN-alpha2b, defined by residues 24-41, 43-49, and 148-158 of IFN-alpha2b. As they presented as corresponding to IFN receptor-binding domains, AB loop and E helix, clone No 26 and 35 were chosen for further characterization and shown to bind to WISH cells. Two peptides corresponding to clone No 26 and 35, designated SP-7(SLSPGLP) and FY-7(FSAPVRY) were shown to compete with GFP-IFN-alpha2b for binding to its receptor and to inhibit the IFN-alpha2b-induced antiviral activity. CONCLUSION: Both IFN-alpha2b antagonist peptides, SP-7 and FY-7, were able to inhibit the IFN-induced antiviral activity, and could be helpful in laying the foundation for the molecular mechanism of the interaction between IFN and its receptor.

[Effects of inhibiting SDF-1 expression by RNA interference on adhesion and drug sensitivity of Jurkat cells co-cultured with bone marrow stromal cells].

OBJECTIVE: To observe the effects of inhibiting stromal cell derived factor-1 (SDF-1) expression by RNA interference (RNAi) on adhesion and drug sensitivity of Jurkat cells co-cultured with bone marrow stromal cells. METHODS: SDF-1 specific short hairpin RNA (shRNA) expressing plasmid was transferred into cultured human acute leukemic bone marrow stromal cells, positive clones were isolated by screening G418 resistance (Group A) , SDF-1 protein level in culture supernatant was detected by enzyme-linked immunosorbent assay (ELISA). The adhesion rates to bone marrow stromal cells layer and the drug sensitivity to doxorubicin of co-cultured Jurkat cells were detected by cell counting and MTT assay, respectively. The un-transfected bone marrow stromal cells of acute leukemia patient (Group B) or normal subject (Group C) were taken as control. RESULTS: The level of secreted SDF-1 protein (pg/10(5) cells/week) in the supernatants of Group A, B and C were 1920 +/- 205, 12,370 +/- 1355 and 6620 +/- 770, respectively. Of co-cultured Jurkat cells in Group A, B and C, the adhesion rates after 24 h co-culturing were (28.8 +/- 2.6)%, (57.4 +/- 3.8)% and (45.2 +/- 4.0)%, respectively, and the IC50 values of doxorubicin were 585, 6162 and 1758 nmol/L, respectively. CONCLUSION: Down-regulating SDF-1 expression of bone marrow stromal cells by RNAi reduces adhesion rates and enhances drug sensitivity to doxorubicin of their co-cultured Jurkat cells.

[Effects of RNA interference inhibiting SDF-1 expression in bone marrow stromal cells on the proliferation and apoptosis of co-cultured Jurkat cells].

OBJECTIVE: To study the effects of RNA interference inhibiting stromal cell derived factor-1 (SDF-1) expression on the proliferation and apoptosis of co-cultured Jurkat cells. METHOD: Inhibition of SDF-1 expression by RNA interference (RNAi) was achieved by transferring SDF-1 specific short hairpin RNA (shRNA) expressing plasmid into cultured human acute leukemic bone marrow stromal cells. Resistant clones were obtained by G418 selection (group A). The concentration of SDF-1 protein in culture supernatant was detected by enzyme-linked immunosorbent assay (ELISA). The population double time (PDT), cell cycles, apoptosis rates and the expressions of PCNA, Bcl-2/Bax, Fas/FasL of co-cultured Jurkat cells were detected by cells counting, flow cytometry. TdT-mediated dUTP nick-end labelling (TUNEL) and immunocytochemistry (ICC), respectively. The un-transfected acute leukemic (group B) and normal (group C) bone marrow stromal cells were taken as controls. RESULTS: The content of SDF-1 protein in supernatant of group A\[(384 +/- 41) pg/ml] was significantly lower than that in group B[(2474 +/- 271) pg/ml] or group C[(1324 +/- 154) pg/ml]. As group A compared with group B and group C, the PDT of co-cultured Jurkat cells was prolonged (group A: 42 h, vs group B: 29 h, group C: 33 h), and G(0)/G(1) stage cells increased [group A: (28.47 +/- 2.39)%, vs group B: (19.43 +/- 2.80)%, group C: (27.15 +/- 2.07)%], S stage cells decreased [group A: (25.57 +/- 1.90)%, vs group B: (74.48 +/- 3.23)%, group C: (60.99 +/- 2.33)%], G(2)/M stage cells increased [group A: (45.96 +/- 3.24)%, vs group B: (6.09 +/- 1.96)%, group C: (11.86 +/- 1.98)%], the apoptosis rate increased [group A: (15.2 +/- 0.8)%, vs group B: (5.4 +/- 0.7)%, group C: (9.5 +/- 0.4)%], and the expressions of PCNA, Bcl-2, Fas decreased; whereas the expressions of Bax and FasL were increased. CONCLUSION: The inhibition of SDF-1 expression in bone marrow stromal cells inhibits the proliferation and promotes the apoptosis of co-cultured Jurkat cells.

[Influence of anti-CXCR4 monoclonal antibody 12G5 on killing effect of cytosine arabinoside to HL-60 cell].

This study was aimed to explore the influence of anti-CXCR4 monoclonal antibody 12G5 on killing effect of cytosine arabinoside (Ara C) to HL-60 cell, and to assess its therapeutic value in marrow residual disease. HL-60 cells were cultured and co-cultured with leukemic stromal cells, and SDF-1 activity was inhibited with 10 microg/ml 12G5, then, killing effects of Ara C on HL-60 cells were investigated by MTT and morphology assay. Curves by MTT assay revealed that in the test group of 20 microg/ml Ara C, A(540) values decreased slowly but straightly, however, in control group A(540) values decreased markedly for the first two days, and increased from day 3 or 4. In the test group of 40 microg/ml Ara C, although increasing at constricted range of 7 - 9 days, A(540) values decreased in whole observing period of 12 days, while in control group A(540) values decreased markedly at day 0-3, and increased from day 4. Furthermore, two curves go across each other at day 5, and continue the increasing tendency. Morphology results showed that in both treated groups, the number of HL-60 cell decreased markedly and increased gradually in control group, but just contrary to test group. It is concluded that 12G5 may weaken the killing effect of Ara C on HL60 cell in earlier period, but reinforce the total killing effect and delay the occurrence of drug resistance simultaneously. Thus 12G5 has the therapeutic potential on marrow residual disease.

[Effects of anti-CXCR4 monoclonal antibody on adhesion and proliferation of human acute myelocytic leukemia cell line HL-60].

BACKGROUND & OBJECTIVE: Stromal cell derived factor-1 (SDF-1), excreted by bone marrow stromal cells, may be involved in shielding of marrow stromal cells from leukemia cells by binding to its receptor CXCR4, but the relation between SDF-1/CXCR4 axis and leukemia cells is unclear. This study was to inhibit activity of SDF-1 by anti-CXCR4 monoclonal antibody 12G5, observe changes of adhesion and proliferation of acute myelocytic leukemia cell line HL-60 co-cultivated with leukemic marrow stromal cells, and to assay potential of inhibiting SDF-1-driven processes on treating marrow residual disease. METHODS: HL-60 cells were co-cultured with leukemic marrow stromal cells, and 10 mug/ml 12G5 was added to block SDF-1 activity. Adhesive state, adhesion rate, apoptosis rate, and cell cycle of HL-60 cells were observed after incubation. Living conditions of HL-60 cells were detected by trypan blue exclusion, cell growth curve was protracted. RESULTS: Adhesion rate of 24-h 12G5-incubated HL-60 cells was (39.4+/-7.9)%, while that of control HL-60 cells was (51.4+/-5.9)% (P< 0.05). G0/G1, S, and G2/M phases of 24-h 12G5-incubated HL-60 cells were (55.2+/-4.9)%, (30.4+/-4.1)%, and (14.4+/-5.2)%, respectively, and apoptosis rate was (9.0+/-1.7)%; while those of control HL-60 cells were (44.7+/-2.2)%, (45.3+/-3.7)%, (10.0+/-2.6)%, and (4.0+/-2.4)%, respectively. T test showed that 12G5 induced more cells entering G0/G1 phase (P< 0.05), and increased cell apoptosis rate(P< 0.05). Compared with control HL-60 cells, survival rate and proliferation of 48-h 12G5-incubated HL-60 cells decreased markedly. CONCLUSION: 12G5 may inhibit adhesion ability and proliferation of HL-60 cells, thus inhibiting SDF-1 activity by 12G5 may be helpful to the treatment of marrow residual disease.